Lipid metabolic adaption to long-term ambient PM2.5 exposure in mice

Emerging evidence has demonstrated that exposure to fine particulate matter (PM2.5) is a risk factor for lipid metabolic disorders in the liver. However, the effects of PM2.5 exposure time duration on hepatic lipid metabolism remain unknown. In this study, C57BL/6 mice were randomly divided into ambient PM2.5 (PM) or filtered air (FA) exposure chamber for short-term (4 weeks) or long-term (24 weeks) exposure via a whole body exposure system. We measured hepatic triglyceride and free fatty acid levels and analyzed the alteration of lipometabolism-related molecules in the liver. We found that triglyceride levels were significantly elevated in both short-term and long-term PM2.5-exposed mice and free fatty acid levels were increased after long-term PM2.5 exposure. Besides, enzymes for lipolysis and fatty acid oxidation in the liver were inhibited after short-term PM2.5 exposure but adaptively enhanced after long-term PM(2.5 )exposure. Furthermore, molecules for fatty acid uptake were down-regulated in the short-term PM2.5-exposed mice whereas molecules for lipid export were induced after long-term PM2.5 exposure. Therefore, ambient PM(2.5 )exposure disturbed hepatic lipid metabolism and the effects varied in different exposure duration. These findings in mice provide new insight into the biological basis of PM2.5-induced human metabolic dysfunction and specific strategies may be applied based on different exposure time periods. (C) 2020 Elsevier Ltd. All rights reserved.

Automated summary

Exposure to PM2.5 has been shown to disrupt hepatic lipid metabolism in mice, with triglyceride and free fatty acid levels increasing significantly. Short-term exposure inhibits enzymes for lipolysis and fatty acid oxidation, while long-term exposure enhances them adaptively. Additionally, short-term exposure decreases molecules for fatty acid uptake while long-term exposure induces molecules for lipid export.